Creative Touch Permanent Makeup and Aesthetics

iPRF (injectable platelet-rich fibrin) is an autologous blood-derived preparation produced by low-speed centrifugation of anticoagulant-free whole blood that yields an injectable concentrate of platelets, leukocytes, fibrinogen, and plasma growth factors. Unlike PRP – which delivers a concentrated but acute growth factor burst on platelet degranulation – iPRF’s fibrinogen-to-fibrin conversion begins at the treatment site following injection, producing a provisional fibrin matrix that releases TGF-β1, PDGF, VEGF, and EGF over 7–14 days as fibrin is enzymatically degraded in vivo. Comparative evidence demonstrates approximately twice the collagen type I production and significantly higher TGF-β1 expression in fibroblast models versus PRP. At Creative Touch, iPRF is used as both a standalone intradermal treatment and as a combination layer with microneedling for facial rejuvenation and hair restoration, replacing our previous PRP protocols in 2025.

Injectable platelet-rich fibrin is the injectable liquid preparation within the broader PRF family. The key distinction from other PRF formats – solid membranes, plugs, and gel preparations – is that iPRF is produced at sufficiently low centrifugation speed and duration that the preparation remains injectable at the point of use. The fibrin polymerisation that defines all PRF preparations does not occur during centrifugation; it begins in vivo, at the treatment site, following injection. This is what separates iPRF from both solid PRF (which polymerises during preparation) and PRP (which contains anticoagulant and does not undergo fibrin formation at all). For the full biological substrate – including fibrin matrix architecture, the PRF preparation family, and growth factor mechanisms – see the PRF entity.

The preparation uses no anticoagulant, no bovine thrombin activator, and no additives of any kind. The final product is concentrated from the patient’s own blood and contains only what was present in it to begin with. This absolute autologous character makes biocompatibility complete and allergic reaction risk effectively zero.

Preparation and Composition

iPRF is produced by centrifuging whole blood at approximately 700 RPM for 3–5 minutes using a horizontal centrifuge rotor. This low-speed, short-duration protocol is deliberately insufficient to sediment platelets and leukocytes into a compact pellet – instead, they concentrate at the interface of the plasma and red cell fractions and are collected within the plasma fraction as an injectable suspension.

The resulting preparation contains:

• Platelets at approximately 2–3× baseline blood concentration – lower than high-speed PRP, but present within a fibrin-forming plasma environment that fundamentally changes their functional context
• Leukocytes – specifically neutrophils and monocytes – which contribute additional growth factors, cytokines, and immunomodulatory signals absent from standard PRP
• Fibrinogen – the soluble plasma protein that converts to fibrin at the injection site, forming the provisional matrix that drives sustained release
• Plasma growth factors – TGF-β1, PDGF, VEGF, EGF, IGF-1, and FGF – present in the plasma fraction prior to any platelet degranulation; their release is substantially amplified by platelet alpha granule secretion following injection
• Plasma proteins – fibronectin, vitronectin, and other matrix proteins that support cell adhesion and migration within the forming fibrin scaffold

Summary: iPRF vs PRP

The Timing Constraint

Because no anticoagulant is used, fibrin polymerisation begins as soon as the preparation is exposed to tissue and body temperature. The working window between centrifugation completion and injection is narrow – the preparation must be used promptly or it becomes too viscous to inject comfortably. Temperature affects polymerisation rate: a cooler environment extends the working window slightly; working at elevated room temperature shortens it.

The timing risk is entirely post-centrifugation. The preparation concern is not collecting iPRF too early during centrifugation – it is waiting too long after the centrifuge stops. This is why iPRF requires more practitioner skill than PRP and why outcomes vary more between clinics than with standardised, anticoagulated PRP protocols. Centrifuge immediately before treatment; inject promptly; do not prepare and set aside.

Clinical Pearl The “too viscous to inject” problem is nearly always a temperature and workflow issue, not a preparation failure. iPRF prepared in a warm room, left in a syringe for several minutes before injection, or drawn up too slowly will begin polymerising prematurely. The solution is not to adjust centrifugation – it is to optimise workflow: centrifuge tube kept cool until draw-up, immediate transfer to syringe, and injection prioritised before any other treatment steps. Practitioners who experience inconsistent iPRF viscosity should audit room temperature and preparation-to-injection elapsed time before adjusting protocol parameters.

Why the Fibrin Matrix Changes the Biology

In standard PRP, platelets degranulate on contact with tissue, releasing their alpha granule contents – essentially all available growth factors – within approximately 15 minutes. The tissue receives a concentrated growth factor signal that is largely resolved within hours. Fibroblasts are activated, but the instructional signal is short-lived relative to the collagen remodelling timeline.

iPRF’s fibrin matrix converts this acute pulse into a sustained signal. As fibrin is degraded by plasmin over 7–14 days, entrapped growth factors are released progressively – TGF-β1 and PDGF maintaining fibroblast activation, VEGF supporting new vessel formation, EGF and IGF-1 supporting keratinocyte renewal and matrix synthesis across the full remodelling period rather than its opening hours. Comparative fibroblast studies show iPRF produces approximately twice the collagen type I protein staining of PRP, with significantly higher TGF-β1, collagen I, and fibronectin mRNA expression – the growth factor signal is not only more sustained but cumulatively more potent.

The leukocyte fraction contributes meaningfully to this outcome. Monocytes recruited within the fibrin scaffold undergo macrophage differentiation and – in the provisional matrix environment – tend toward M2 (anti-inflammatory, pro-regenerative) polarisation, producing additional TGF-β and VEGF that amplifies the platelet-derived signal. This is a mechanism PRP does not replicate because leukocytes are typically reduced or excluded in PRP protocols designed to minimise post-treatment redness.